Field of the Invention
The present invention is directed to an intra-pericardial surgically introduced positioning structure that is disposed and structured to repetitively assume an expanded orientation and a contracted orientation. As such, a repetitively and temporarily “lifting” or “shaping” force is exerted on the exterior of the myocardium in synchronization with the heartbeat thereby positioning the leaflets of the mitral valve to close to a sufficient degree to eliminate or restrict mitral regurgitation.
Description of the Related Art
As clearly disclosed in the prior art schematic representation of FIG. 1, the human heart is a four chambered pump that moves blood efficiently through the vascular system. During normal operation, blood enters the heart through the vena cava and flows into the right atrium. Thereafter, blood flows from the right atrium through the tricuspid valve and into the right ventricle. Upon contraction of the right ventricle, blood is forced through the pulmonic or pulmonary valve and into the lungs for oxygenation. The oxygenated blood returns from the lungs and enters the heart through the left atrium and passes through the mitral valve into the left ventricle. Upon contraction of the left ventricle the blood therein flows through the aortic valve and into the aorta and throughout the vascular system.
As indicated, the mitral valve is disposed in flow regulating communication between the left atrium and the left ventricle. The structural and/or operative components of the mitral valve comprises two valve leaflets, the mitral valve annulus, which forms a ring that supports the valve leaflets; papillary muscles, which tether the valve leaflets to the left ventricle wall, thereby preventing them from prolapsing back into the left atrium. Chordae tendineae serve to connect the mitral valve leaflets to the papillary muscles thereby further preventing the leaflets from prolapsing back into the left atrium. A dysfunction of any of the described mitral valve apparatus can cause “mitral regurgitation”. Mitral regurgitation is a disorder of the heart in which the leaflets of the mitral valve do not close properly when the heart pumps out blood. This abnormal leaking of blood from the left ventricle, through the mitral valve and, into the left atrium when the left ventricle contracts, results in the “regurgitation” of blood back into the left atrium. It is generally recognized in the medical profession that mitral regurgitation is the second most common form of valvular heart disease.
As generally set forth above, when properly functioning, the anterior and posterior valve leaflets of the mitral valve overlap during contraction of the left ventricle and prevent blood from flowing back into the left atrium. This overlap of the two leaflets leaning upon each other is called the “coaptation” and absorbs most of the strain on the mitral apparatus during the ventricular contraction. However, when the mitral valve malfunctions, due to various cardiac diseases, the leaflets are no longer coapting resulting in the mitral valve remaining partially open during ventricular contraction. In turn this allows the aforementioned “regurgitation” of the blood back into the left atrium, as generally set forth above. When the mitral valve does not close hermetically during the ventricular contraction, the aforementioned back flow of blood to the atrium and the pulmonary vasculature, results in a deleterious condition. More specifically, this condition increases the work load to the heart and may lead to heart failure.
The mitral valve is intended to open fully so as to provide no resistance to the blood stream progressing from the left atrium (LA) into the left ventricle (LV) during diastoly (the ventricular relaxation phase) and to close fully during the systoly (the ventricular ejection phase) so as to prevent the blood from flowing back into the atrium and into the pulmonary venous circulation. The role of the mitral valve is therefore to ensure antegrade progression of the blood through the left cardiac chambers. It works in synchrony with the three other heart valves that are ensuring the same function between the right atrium (RA) i.e. the pulmonic valve and downstream to the mitral valve, between the left ventricle and the aorta i.e. the aortic valve at the junction.
From a mechanical standpoint the mitral valve has to face high gradients of pressure during the ventricular contraction to hold up against a pressure head of about 100 mm of mercury (Hg) or more, which is substantially the peak pressure in the LV being usually superior or equal to 110 mmHg and the one in the atrium around 8 mmHg. This strain is absorbed mostly by the coaptation of the two mitral leaflets when closed, leaning on each other with a contact height around 10 mm over the entire length of the mitral coaptation line. The coaptation of the leaflets depends on the adequate anatomy (integrity of their structures) and adequate function of 5 components, which are 1. the mitral annulus, 2. the anterior and posterior leaflets, 3. the mitral chordae, 4. the papillary muscles (PPM) and 5. the ventricular walls themselves. Any congenital malformation or acquired lesion of one or more of these components can lead to a mitral insufficiency—also known as mitral regurgitation (MR) or, as emphasized herein, a failure of the mitral valve to hermetically close during the ventricular contraction and the leaking of a variable amount of blood back into the LA.
This situation is correlated with a poor outcome for the patient, since it increases the workload to the heart, as well as it increases the left atrial and ventricular chambers volumes. Furthermore, the existence of severe mitral regurgitation and ventricular dilation generate a vicious cycle in which MR begets more MR. Indeed, when the ventricle increases in size the distance between the papillary muscles increases, tethering the mitral chordae and impeding their full motion up to the plane of the annulus. This pathophysiological continuum leads to heart failure, pulmonary hypertension, atrial fibrillation and ultimately death.
Known treatment for MR comprises the administration of pharmacological drugs and the fixing the regurgitation by either, a surgical repair (the vast majority of the cases >98%) including a surgical repair or replacement of the valve or in some selected cases, using an emerging percutaneous technology that is still under evaluation (the Mitraclip®). Although there is a considerable trend to fix the MR as early as possible in its natural course, the indication and timing of the intervention rely also on the etiology of the condition, as well as on the functional anatomy and structural damage to the valve and the ventricle.
One particular case of mitral regurgitation targeted by the present invention is called ischemic mitral regurgitation (IMR). Ischemia to the heart relates to an insufficient blood supply to the myocardium because of narrowed (stenosed) coronary arteries. This condition is extremely prevalent and the number one killer in the USA. The natural history of coronary artery disease (stenosis) is to evolve towards acute vessel occlusion leading to acute myocardial infarction (myocardial necrosis i.e. cellular death secondary to cellular asphyxia in the territory irrigated by the occluded artery). The onset of mitral ischemia is a very bad prognostic factor in the acute phase of myocardial infarction.
Repairing ischemic mitral insufficiency poses particular problems and challenges that have been approached in different ways. However, many of such approaches have been disappointing on the very mid-term, with most studies reporting ≧40% of failure rate only two years after the surgery. Most of the proposed solutions are targeted towards the annulus and the leaflets although the mitral valve apparatus is anatomically normal and the functional problem is of ventricular origin. Indeed, the scar tissue replacing the death of the myocardium during the body repair process is immobile and remains distended in systoly. Therefore, by tethering as above-mentioned, the mobility of the entire mitral apparatus attached to it is impaired resulting in the PPM, the chordae and the leaflets being pulled “down” or away from the plane of the mitral annulus. This impeaches the leaflet (usually the posterior leaflet) to reach the point where it should coapt with its anterior counterpart. More technically, this mechanism corresponds to a type IIIb according to Carpentier's classification. It is an extremely frequent phenomenon.
Similarly other, “non-ischemic” etiologies leading to mitral regurgitation, such as for example idiopathic cardiomyopathy, could benefit from the implementation and practice of one or more to the embodiments of the present invention, as described in detail herein. An alternative solution allowing an easier, safer and possibly more durable reduction or disappearance of the mitral regurgitation has been sought, based on the premise that the IMR is a “ventricular disease” thereby suggesting a ventricular solution rather than concentrating on an approach to a normal annulus or normal leaflet.
Accordingly, there is a need in the medical arts for appropriate instrumentation, method and/or system of overcoming heart valve malfunctions, specifically including mitral regurgitation, as described above.